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Volume 61, Issue 4

isolates from Greek children express type 2 and type 1 Lewis and α1,6-glucan antigens in conjunction with a functional type IV secretion system Free

Abstract

infection is often acquired in childhood and can persist for life. Previous studies in adult patients have shown that isolates from North American and European hosts express predominantly type 2 Lewis x (Le) and Le epitopes, while Asian strains have the capacity to express type 1 Le and Le structures. In order to understand the influence of environmental and host factors on the expression of Le antigens, we analysed 50 Greek isolates from symptomatic children. Both CagA-positive and -negative strains were evaluated. The expression of Le antigens was determined by whole-cell indirect ELISA (WCE), and LPS profiles were assessed by gel electrophoresis and immunoblotting. Occurrence of Le and/or Le antigens was confirmed in 35 of the isolates (70 %) while 15 of the isolates were non-typable. It was found that 11 of the paediatric isolates had the propensity to express type 1 Le blood-group antigen (22 %), a feature relatively uncommon in isolates from adults. One strain expressed both Le and Le antigens. The majority of the isolates (49/50, 98 %) expressed α1,6-glucan, an antigenic non-Le determinant present in the outer core region of LPS. All Le- and Le-expressing strains also carried a functional pathogenicity island-encoding a type IV secretion system, capable of translocating CagA protein, as well as the allele, suggesting that Le and Le epitopes may aid the persistence of more aggressive strains. No association between bacterial virulence characteristics and the histopathological observations was evident.

  • Received:
  • Accepted:
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© 2012 National Research Council of Canada
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2012-04-01
2024-04-19
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Helicobacter pylori isolates from Greek children express type 2 and type 1 Lewis and α1,6-glucan antigens in conjunction with a functional type IV secretion system
J. Med. Microbiol. 61, 559 (2012); https://doi.org/10.1099/jmm.0.038729-0
/content/journal/jmm/10.1099/jmm.0.038729-0
/content/journal/jmm/10.1099/jmm.0.038729-0
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